Published online Feb 21, 2017. doi: 10.3748/wjg.v23.i7.1203
Peer-review started: November 15, 2016
First decision: December 19, 2016
Revised: December 27, 2016
Accepted: January 11, 2017
Article in press: January 11, 2017
Published online: February 21, 2017
Processing time: 97 Days and 3.1 Hours
To investigate the antioxidant effect of caffeic acid phenethyl ester (CAPE) in hepatic stellate cell-T6 (HSC-T6) cells cultured in vitro and the potential mechanisms.
HSC-T6 cells were cultured in vitro and treated with various concentrations of CAPE for 24, 48 and 72 h, respectively. Cell proliferation was investigated using the MTT assay, and cell ultrastructural alterations were observed by transmission electron microscopy. Flow cytometry was employed to investigate the effects of CAPE on apoptosis and the levels of reactive oxygen species in HSC-T6 cells cultured in vitro. An enzyme immunoassay instrument was used to evaluate antioxidant enzyme expression. The effect on α-smooth muscle actin was shown using immunofluorescence. Gene and protein levels of Nrf2, related factors, and mitogen activated protein kinases (MAPKs), in HSC-T6 cells were detected using RT-PCR and Western blot, respectively.
CAPE inhibited the proliferation and activation of HSC-T6 cells cultured in vitro. CAPE increased the antioxidant levels and the translocation of Nrf2 from the cytoplasm to the nucleus in HSC-T6 cells. Moreover, the phosphorylation of MAPKs in cells decreased in response to CAPE. Interestingly, CAPE-induced oxidative stress in the cells was significantly attenuated by pretreatment with MAPKs inhibitors.
CAPE inhibits cell proliferation and up-regulates the antioxidant levels in HSC-T6 cells partly through the Nrf2-MAPKs signaling pathway.
Core tip: Liver fibrosis is a pathological response to hepatocyte injury, including oxidative stress, which is a primary mechanism of liver damage. Caffeic acid phenethyl ester (CAPE) is a phenolic compound extracted from honeybee propolis that has strong biological properties in liver protection and as an antioxidant and anti-fibrosis agent. It has been used in the treatment of several diseases. In this study, we investigated the antioxidant effect of CAPE in HSC-T6 cells and its potential mechanism. Our results demonstrated that CAPE inhibited cell proliferation and up-regulated the antioxidant levels in HSC-T6 cells partly through the Nrf2-MAPKs signaling pathway.